1. Field of the Invention
This invention relates generally to devices for resizing ventricle and related methods for placing the devices. More particularly, it relates to sizing devices for reducing the ventricular volume to improve the heart's pumping action. The devices and methods of the present invention are directed toward thoracoscopy or subxiphoid techniques used to facilitate sizing of the ventricles.
2. Prior Art
Heart failure (HF), the heart's inability to pump an adequate volume of blood to the tissues, is the only major cardiovascular condition that continues to increase in incidence in the United States. Approximately 5 million patients are currently diagnosed with HF in the United States. The American Heart Association estimates that 550,000 new HF cases develop each year. This condition is responsible for an estimated 900,000 hospitalizations annually—more than any other medical condition among the elderly. Approximately 6.5 million hospital days each year are attributed to and related to HF and as many as one third of those patients are readmitted for treatment of symptom recurrence within 90 days. Thus, it is not surprising that the cost of providing advanced medical care for the millions of patients suffering from HF is extraordinarily high—now estimated at more than $38 billion annually.
In certain pathological conditions, the ventricles of the heart become ineffective in pumping the blood, causing a back-up of pressure in the vascular system behind the ventricle. The reduced effectiveness of the heart is usually due to an enlargement of the heart. Coronary artery disease causes approximately 60% of congestive heart failure. Acute myocardial infarction (AMI) due to obstruction of a coronary artery is a common initiating event that can lead ultimately to heart failure. A myocardial ischemia may, for example, cause a portion of a myocardium of the heart to lose its ability to contract. Prolonged ischemia can lead to infarction of a portion of the myocardium (heart muscle) wherein the heart muscle dies and becomes scar tissue. Once this tissue dies, it no longer functions as a muscle and cannot contribute to the pumping action of the heart. When the heart tissue is no longer pumping effectively, that portion of the myocardium is said to be hypokinetic, meaning that it is less contractile than the uncompromised myocardial tissue. As this situation worsens, the local area of compromised myocardium may in fact bulge out as the heart contracts, further decreasing the hearts ability to move blood forward. When local wall motion moves in this way it is said to be dyskinetic. The dyskinetic portion of the myocardium may stretch and eventually form an aneurysmic bulge.
One problem with a large dilated left ventricle is that there is a significant increase in wall tension and/or stress both during diastolic filling and during systolic contraction. In a normal heart, the adaptation of muscle hypertrophy (thickening) and ventricular dilatation maintain a fairly constant wall tension for systolic contraction. However, in a failing heart, the ongoing dilatation is greater than the hypertrophy and the result is a rising wall tension requirement for systolic contraction. This is felt to be an ongoing insult to the muscle myocyte resulting in further muscle damage. In response, the heart tissue remodels to accommodate the chronically increased filling pressures, further increasing the work that the now-compromised myocardium must perform. This vicious cycle of cardiac failure results in the symptoms of congestive heart failure such as shortness of breath on exertion, edema in the periphery, nocturnal dypsnia (a characteristic shortness of breath that occurs at night after going to bed), weight gain, and fatigue, to name a few. The increase in wall stress also occurs during diastolic filling. The stress increase requires a larger among of oxygen supply, which can result in exhaustion of the myocardium leading to a reduced cardiac output of the heart.
The incidence of ischemic dilated cardiomyopathy is increasing, not only as a consequence of the aging of the population, but also because effective emergency interventions for otherwise fatal acute coronary events are extending the lives of many patients with ischemic congestive heart failure (CHF). Despite the major advances in both medical and surgical therapy, the management of patients with coronary artery disease and left ventricular (LV) dysfunction continues to be challenging due to the complex and multifactorial pathophysiology of this condition.
Since heart transplantation, when indicated, continues to be limited by several factors, conventional surgical treatment for ischemic cardiomyopathy has gained increasing attention in recent years and a variety of therapeutic interventions have been developed or optimized.
It has been demonstrated that myocardial revascularization and valve repair are capable of improving left ventricular function.
Recent efforts have concentrated on improving left ventricular function by means of surgical methods aimed at ventriculoplasty with or without a reduction in ventricular volume.
Prior treatments for heart failure associated with such dilatation fall into three general categories. The first being pharmacological treatment, for example, diuretics and ACE inhibitors. The second being assist devices, for example, pumps. Finally, effective surgical treatments also have been performed with, for example, the Dor or Jatene procedure, or left ventricular reconstruction (LVR), which requires the use of cardiopulmonary bypass (CPB) machine.
Many patients who would benefit from left ventricular reconstruction are the least likely to withstand the effects of CPB due to age, poor ejection fraction, or other cardiovascular disease. Therefore, there remains a need for an efficient device and method for reducing ventricular volume.